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About Me

Hi! My name is Qadoshyah and I'm the oldest of 11 kids. I live on a ranch in the beautiful country of Northeastern Oklahoma with my family. We are a large household with so many kids that we have various projects going on: We raise goats, pigs, sheep, and rabbits (I raise the rabbits - cute little mini lops) on our 44 acre ranch. Our ranch is also home to bullmastiffs, chickens, guinea hens, ducks, llamas, a donkey, a bottle calf, and several ranch dogs and livestock guardian dogs. The youngest two kids are boy/girl twins born in Feb. '05. The boy happens to have Down syndrome. He is such a blessing to our family :)! Our whole family is also gluten-free, which adds another interesting aspect to our large, active family. We also cook dairy-free & corn-free due to allergies a few kids have. Some of the family is also on the GAPS diet to restore gut health.

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Tuesday, July 9, 2013

This was posted on the DSTNI listserv by Richard and I thought I'd share here:

Drug Improves
Cognitive Function in Mouse Model of Down Syndrome

July 2, 2013 — An existing FDA-approved drug improves cognitive function in a
mouse model of Down syndrome, according to a new study by researchers at the
Stanford University School of Medicine.

The drug, an asthma medication called formoterol, strengthened nerve
connections in the hippocampus, a brain center used for spatial navigation,
paying attention and forming new memories, the study said. It also improved
contextual learning, in which the brain integrates spatial and sensory
information.

Both hippocampal function and contextual learning, which are impaired in Down
syndrome, depend on the brain having a good supply of the neurotransmitter
norepinephrine. This neurotransmitter sends its signal via several types of
receptors on the neurons, including a group called beta-2 adrenergic receptors.

"This study provides the initial proof-of-concept that targeting beta-2
adrenergic receptors for treatment of cognitive dysfunction in Down syndrome
could be an effective strategy," said Ahmed Salehi, MD, PhD, the study's
senior author and a clinical associate professor of psychiatry and behavioral
sciences. The study will be published online July 2 in Biological Psychiatry.

Down syndrome, which is caused by an extra copy of chromosome 21, results in
both physical and cognitive problems. While many of the physical issues, such
as vulnerability to heart problems, can now be treated, no treatments exist for
poor cognitive function. As a result, children with Down syndrome fall behind
their peers' cognitive development. In addition, adults with Down syndrome
develop Alzheimer's-type pathology in their brains by age 40. Down syndrome
affects about 400,000 people in the United States and 6 million worldwide.

In prior Down syndrome research, scientists have seen deterioration of the
brain center that manufactures norepinephrine in both people with Down syndrome
and its mouse model. Earlier work by Salehi's team found that giving a
norepinephrine precursor could improve cognitive function in a mouse model
genetically engineered to mimic Down syndrome.

The new study refined this work by targeting only one group of receptors that
respond to norepinephrine: the beta-2 adrenergic receptors in the brain. The
researchers began by giving mice a compound that blocks the action of beta-2
adrenergic receptors outside the brain. They then gave the mice formoterol, a
drug that can partially cross the blood-brain barrier and that was already
known to activate beta-2 adrenergic receptors. Because people with Down
syndrome are prone to heart problems, the researchers avoided activating a
different group of norepinephrine-sensitive receptors, the beta-1 adrenergic
receptors, which predominate in the heart.

The scientists saw improvement on a standard test of contextual learning in
mice. In contextual learning, the brain integrates sensory and spatial
information to remember the layout of a complex environment: for instance, a
person using sounds, smells and sights to remember the location of a store in a
shopping mall is using contextual learning. The researchers also saw more
synapses and a more complex structure of dendrites, the nerves' outgoing ends,
in the hippocampus after the affected mice received formoterol.

"The fact that such a short period of giving medication can make these
neurons much more complex is very interesting," Salehi said, noting that
mice in the study received the drug for a maximum of two weeks.

Further tests will be needed to determine whether formoterol might be an
appropriate treatment for people with Down syndrome or whether to use another
drug that activates the same receptors, Salehi said. The dose used in this
study was many times higher than that used for asthma treatment, he cautioned,
so it is not known whether it is safe. A lower dose might work, or other drugs
that affect beta-2 adrenergic receptors might be safer and more effective in
humans. Researchers also want to explore what parts of learning -- taking in
new information, remembering it or both -- are affected by the drug treatment.

Prior research to improve cognitive function in children with Down syndrome has
sometimes raised concerns from families that cognitive treatments would alter
positive attributes of these children's personalities, but Salehi said that is
not the goal of his team's research.

"Our aim is to enable these children to do better in school," Salehi
said. "It is absolutely not to change their personalities or the way they
react to society." Changing a child's personality would be much more complicated
than activating a subgroup of receptors in the brain, he said.Tweet